際際滷shows by User: vaishaliwasnik / http://www.slideshare.net/images/logo.gif 際際滷shows by User: vaishaliwasnik / Tue, 29 Aug 2023 08:23:24 GMT 際際滷Share feed for 際際滷shows by User: vaishaliwasnik Tablets.pptx /vaishaliwasnik/tabletspptx-260284539 tablets-230829082324-42d128f0
Tablets- Tablets are unit dosage form in which one usual dose of the drug has been accurately placed. Advantages Unit dosage form, greatest dose precision and least content variability. Lowest cost Lightest and most compact form Easiest and cheapest to package Product identification is also cheap no additional processing required Provide greatest ease of swallowing. Special release profile can formed Chemical, Mechanical and microbiologic stability. Suitable for large scale production Disadvantages Some drugs not suitable for compression (amorphous, flocculents , low density ) Drugs with por wetting , slow disslution, intermediate to large dosage are difficult to formulate into tablet. Bitter tasting, objectional odor, drugs sensitive to oxygen may require coating ( capsule prefer at low cost) Tablets used for Ingestion Compressed Tablets or Standard compressed Tablets Standard uncoated tablets made by compression- wet granulations, double compaction or direct compression. Rapid disintegration & drug release Most of tablets containing drugs which gives local effect.( GIT- Water insoluble drugs Antacids and adsorbents) Some drugs produced systemic effect ( aqueous solubility- Disintegrate and dissolve in GI contents) 2. Multiple compressed Tablets Either two components or three components systems A tablet within a tablet Tablet within tablet within a tablet. 3. Chewable Tablets Chew in mouth prior to swallowing & not intended to be swallowed intact. Infants and children or for elderly Bitter and foul tasting drugs not suitable. E.g.- Antacid tablets ( large dose of antacid can be given and better acid neutralization) 4. Sugar and Chocolate coated 5. Film coated Tablets Polymers such as Hydroxypropyl cellulose (HPC), Hydroxypropyl methyl cellulose(HPMC), widely used with suitable plasticizer. Advantages Better mechanical strength Avoid sugar for significant segments of population Retain debossed markings Tasteless Tablet - Disadvantge Physical appearnce ( Elegancy) not match with sugar coated tablets. 6. Repeat action Tablets The core of tablet is coated with shellac or an enteric polymer so drug not releases into stomach. Second dose added into sugar coatings. 7. Delayed action And Enteric coated Tablets Enteric coated Tablets are a type of delayed action tablet. But not all types of delayed type of tablets are enteric. Why enteric coating? Some drugs irritate gastric mucosa (Aspirin) Some drugs destroyed in stomach (Erythromycin) For local effect in intestine( antibacterial, Vermifuge) Cellulose acetate phthalate, polyvinyl acetate phthalate, HPMC phthalate Acid esters ( insoluble in GI media) Esterases in intestinal fluid break down ester linkages. 8. Controlled release Tablets Tablets used for oral cavity 1. Buccal & Sublingual Tablets These tablets are small & somewhat flat Buccal tablets intended to be held between the cheek and teeth or in the cheek pouch Sublingual tablets intended to held beneath the tongue. Drugs admi]]>

Tablets- Tablets are unit dosage form in which one usual dose of the drug has been accurately placed. Advantages Unit dosage form, greatest dose precision and least content variability. Lowest cost Lightest and most compact form Easiest and cheapest to package Product identification is also cheap no additional processing required Provide greatest ease of swallowing. Special release profile can formed Chemical, Mechanical and microbiologic stability. Suitable for large scale production Disadvantages Some drugs not suitable for compression (amorphous, flocculents , low density ) Drugs with por wetting , slow disslution, intermediate to large dosage are difficult to formulate into tablet. Bitter tasting, objectional odor, drugs sensitive to oxygen may require coating ( capsule prefer at low cost) Tablets used for Ingestion Compressed Tablets or Standard compressed Tablets Standard uncoated tablets made by compression- wet granulations, double compaction or direct compression. Rapid disintegration & drug release Most of tablets containing drugs which gives local effect.( GIT- Water insoluble drugs Antacids and adsorbents) Some drugs produced systemic effect ( aqueous solubility- Disintegrate and dissolve in GI contents) 2. Multiple compressed Tablets Either two components or three components systems A tablet within a tablet Tablet within tablet within a tablet. 3. Chewable Tablets Chew in mouth prior to swallowing & not intended to be swallowed intact. Infants and children or for elderly Bitter and foul tasting drugs not suitable. E.g.- Antacid tablets ( large dose of antacid can be given and better acid neutralization) 4. Sugar and Chocolate coated 5. Film coated Tablets Polymers such as Hydroxypropyl cellulose (HPC), Hydroxypropyl methyl cellulose(HPMC), widely used with suitable plasticizer. Advantages Better mechanical strength Avoid sugar for significant segments of population Retain debossed markings Tasteless Tablet - Disadvantge Physical appearnce ( Elegancy) not match with sugar coated tablets. 6. Repeat action Tablets The core of tablet is coated with shellac or an enteric polymer so drug not releases into stomach. Second dose added into sugar coatings. 7. Delayed action And Enteric coated Tablets Enteric coated Tablets are a type of delayed action tablet. But not all types of delayed type of tablets are enteric. Why enteric coating? Some drugs irritate gastric mucosa (Aspirin) Some drugs destroyed in stomach (Erythromycin) For local effect in intestine( antibacterial, Vermifuge) Cellulose acetate phthalate, polyvinyl acetate phthalate, HPMC phthalate Acid esters ( insoluble in GI media) Esterases in intestinal fluid break down ester linkages. 8. Controlled release Tablets Tablets used for oral cavity 1. Buccal & Sublingual Tablets These tablets are small & somewhat flat Buccal tablets intended to be held between the cheek and teeth or in the cheek pouch Sublingual tablets intended to held beneath the tongue. Drugs admi]]>
Tue, 29 Aug 2023 08:23:24 GMT /vaishaliwasnik/tabletspptx-260284539 vaishaliwasnik@slideshare.net(vaishaliwasnik) Tablets.pptx vaishaliwasnik Tablets- Tablets are unit dosage form in which one usual dose of the drug has been accurately placed. Advantages Unit dosage form, greatest dose precision and least content variability. Lowest cost Lightest and most compact form Easiest and cheapest to package Product identification is also cheap no additional processing required Provide greatest ease of swallowing. Special release profile can formed Chemical, Mechanical and microbiologic stability. Suitable for large scale production Disadvantages Some drugs not suitable for compression (amorphous, flocculents , low density ) Drugs with por wetting , slow disslution, intermediate to large dosage are difficult to formulate into tablet. Bitter tasting, objectional odor, drugs sensitive to oxygen may require coating ( capsule prefer at low cost) Tablets used for Ingestion Compressed Tablets or Standard compressed Tablets Standard uncoated tablets made by compression- wet granulations, double compaction or direct compression. Rapid disintegration & drug release Most of tablets containing drugs which gives local effect.( GIT- Water insoluble drugs Antacids and adsorbents) Some drugs produced systemic effect ( aqueous solubility- Disintegrate and dissolve in GI contents) 2. Multiple compressed Tablets Either two components or three components systems A tablet within a tablet Tablet within tablet within a tablet. 3. Chewable Tablets Chew in mouth prior to swallowing & not intended to be swallowed intact. Infants and children or for elderly Bitter and foul tasting drugs not suitable. E.g.- Antacid tablets ( large dose of antacid can be given and better acid neutralization) 4. Sugar and Chocolate coated 5. Film coated Tablets Polymers such as Hydroxypropyl cellulose (HPC), Hydroxypropyl methyl cellulose(HPMC), widely used with suitable plasticizer. Advantages Better mechanical strength Avoid sugar for significant segments of population Retain debossed markings Tasteless Tablet - Disadvantge Physical appearnce ( Elegancy) not match with sugar coated tablets. 6. Repeat action Tablets The core of tablet is coated with shellac or an enteric polymer so drug not releases into stomach. Second dose added into sugar coatings. 7. Delayed action And Enteric coated Tablets Enteric coated Tablets are a type of delayed action tablet. But not all types of delayed type of tablets are enteric. Why enteric coating? Some drugs irritate gastric mucosa (Aspirin) Some drugs destroyed in stomach (Erythromycin) For local effect in intestine( antibacterial, Vermifuge) Cellulose acetate phthalate, polyvinyl acetate phthalate, HPMC phthalate Acid esters ( insoluble in GI media) Esterases in intestinal fluid break down ester linkages. 8. Controlled release Tablets Tablets used for oral cavity 1. Buccal & Sublingual Tablets These tablets are small & somewhat flat Buccal tablets intended to be held between the cheek and teeth or in the cheek pouch Sublingual tablets intended to held beneath the tongue. Drugs admi <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/tablets-230829082324-42d128f0-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Tablets- Tablets are unit dosage form in which one usual dose of the drug has been accurately placed. Advantages Unit dosage form, greatest dose precision and least content variability. Lowest cost Lightest and most compact form Easiest and cheapest to package Product identification is also cheap no additional processing required Provide greatest ease of swallowing. Special release profile can formed Chemical, Mechanical and microbiologic stability. Suitable for large scale production Disadvantages Some drugs not suitable for compression (amorphous, flocculents , low density ) Drugs with por wetting , slow disslution, intermediate to large dosage are difficult to formulate into tablet. Bitter tasting, objectional odor, drugs sensitive to oxygen may require coating ( capsule prefer at low cost) Tablets used for Ingestion Compressed Tablets or Standard compressed Tablets Standard uncoated tablets made by compression- wet granulations, double compaction or direct compression. Rapid disintegration &amp; drug release Most of tablets containing drugs which gives local effect.( GIT- Water insoluble drugs Antacids and adsorbents) Some drugs produced systemic effect ( aqueous solubility- Disintegrate and dissolve in GI contents) 2. Multiple compressed Tablets Either two components or three components systems A tablet within a tablet Tablet within tablet within a tablet. 3. Chewable Tablets Chew in mouth prior to swallowing &amp; not intended to be swallowed intact. Infants and children or for elderly Bitter and foul tasting drugs not suitable. E.g.- Antacid tablets ( large dose of antacid can be given and better acid neutralization) 4. Sugar and Chocolate coated 5. Film coated Tablets Polymers such as Hydroxypropyl cellulose (HPC), Hydroxypropyl methyl cellulose(HPMC), widely used with suitable plasticizer. Advantages Better mechanical strength Avoid sugar for significant segments of population Retain debossed markings Tasteless Tablet - Disadvantge Physical appearnce ( Elegancy) not match with sugar coated tablets. 6. Repeat action Tablets The core of tablet is coated with shellac or an enteric polymer so drug not releases into stomach. Second dose added into sugar coatings. 7. Delayed action And Enteric coated Tablets Enteric coated Tablets are a type of delayed action tablet. But not all types of delayed type of tablets are enteric. Why enteric coating? Some drugs irritate gastric mucosa (Aspirin) Some drugs destroyed in stomach (Erythromycin) For local effect in intestine( antibacterial, Vermifuge) Cellulose acetate phthalate, polyvinyl acetate phthalate, HPMC phthalate Acid esters ( insoluble in GI media) Esterases in intestinal fluid break down ester linkages. 8. Controlled release Tablets Tablets used for oral cavity 1. Buccal &amp; Sublingual Tablets These tablets are small &amp; somewhat flat Buccal tablets intended to be held between the cheek and teeth or in the cheek pouch Sublingual tablets intended to held beneath the tongue. Drugs admi
Tablets.pptx from vaishaliwasnik
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Calcification.pptx /slideshow/calcificationpptx/257970140 calcification-230523041922-1e8dfa73
Deposition of calcium salts in tissues other than osteoid or enamel is called pathologic or heterotopic calcification Two distinct types of pathologic calcification are recognised: Dystrophic calcifi cation is characterised by deposition of calcium salts in dead or degenerated tissues with normal calcium metabolism and normal serum calcium level. Metastatic calcifi cation, on the other hand, occurs in apparently normal tissues and is associated with deranged calcium metabolism and hypercalcaemia. Etiopathogenesis The two types of pathologic calcifi cation result from distinctly different etiologies and mechanisms. DYSTROPHIC CALCIFICATION As apparent from definition, dystrophic calcification may occur due to 2 types of causes: Calcification in dead tissue. Calcification of degenerated tissue. Calcification in dead tissue Caseous necrosis in tuberculosis is the most common site for dystrophic calcification. Living bacilli may be present even in calcified tuberculous lesions, lymph nodes, lungs, etc 2. Liquefaction necrosis in chronic abscesses may get calcified. 3. Fat necrosis following acute pancreatitis or traumatic fat necrosis in the breast results in deposition of calcium soaps. 4. Gamna-Gandy bodies in chronic venous congestion (CVC) of the spleen is characterised by calcific deposits admixed with haemosiderin on fi brous tissue. 5. Infarcts may sometimes undergo dystrophic calcifi cation. 6. Th rombi, especially in the veins, may produce phleboliths. 7. Haematomas in the vicinity of bones may undergo dystrophic calcification. 8. Dead parasites like in hydatid cyst, Schistosoma eggs, and cysticercosis are some of the examples showing dystrophic calcifi cation. 9. Microcalcifi cation in breast cancer detected by mammography. 10. Congenital toxoplasmosis involving the central nervous system visualised by calcifi cation in the infant brain. Calcification in degenerated tissues 1. Dense old scars may undergo hyaline degeneration and subsequent calcifi cation. 2. Atheromas in the aorta and coronaries frequently undergo calcifi cation. 3. M旦nckebergs sclerosis shows calcifi cation in the degenerated tunica media of muscular arteries in elderly people . 4. Stroma of tumours such as uterine fi broids, breast cancer, thyroid adenoma, goitre etc show calcification. 5. Goitre of the thyroid may show presence of calcifi cation in areas of degeneration. 6. Some tumours show characteristic spherules of calcification called psammoma bodies or calco spherites such as in meningioma, papillary serous cystadeno carcinoma of the ovary and papillary carci noma of the thyroid. 7. Cysts which have been present for a long time may show calcification of their walls e.g. epidermal and pilar cysts. 8. Calcinosiscutis is a condition of unknown cause in which there are irregular nodular deposits of calcium salts in the skin and subcutaneous tissue. 9. Senile degenerative changes may be accompanied by dystrophic calcification such as in costal cartilages]]>

Deposition of calcium salts in tissues other than osteoid or enamel is called pathologic or heterotopic calcification Two distinct types of pathologic calcification are recognised: Dystrophic calcifi cation is characterised by deposition of calcium salts in dead or degenerated tissues with normal calcium metabolism and normal serum calcium level. Metastatic calcifi cation, on the other hand, occurs in apparently normal tissues and is associated with deranged calcium metabolism and hypercalcaemia. Etiopathogenesis The two types of pathologic calcifi cation result from distinctly different etiologies and mechanisms. DYSTROPHIC CALCIFICATION As apparent from definition, dystrophic calcification may occur due to 2 types of causes: Calcification in dead tissue. Calcification of degenerated tissue. Calcification in dead tissue Caseous necrosis in tuberculosis is the most common site for dystrophic calcification. Living bacilli may be present even in calcified tuberculous lesions, lymph nodes, lungs, etc 2. Liquefaction necrosis in chronic abscesses may get calcified. 3. Fat necrosis following acute pancreatitis or traumatic fat necrosis in the breast results in deposition of calcium soaps. 4. Gamna-Gandy bodies in chronic venous congestion (CVC) of the spleen is characterised by calcific deposits admixed with haemosiderin on fi brous tissue. 5. Infarcts may sometimes undergo dystrophic calcifi cation. 6. Th rombi, especially in the veins, may produce phleboliths. 7. Haematomas in the vicinity of bones may undergo dystrophic calcification. 8. Dead parasites like in hydatid cyst, Schistosoma eggs, and cysticercosis are some of the examples showing dystrophic calcifi cation. 9. Microcalcifi cation in breast cancer detected by mammography. 10. Congenital toxoplasmosis involving the central nervous system visualised by calcifi cation in the infant brain. Calcification in degenerated tissues 1. Dense old scars may undergo hyaline degeneration and subsequent calcifi cation. 2. Atheromas in the aorta and coronaries frequently undergo calcifi cation. 3. M旦nckebergs sclerosis shows calcifi cation in the degenerated tunica media of muscular arteries in elderly people . 4. Stroma of tumours such as uterine fi broids, breast cancer, thyroid adenoma, goitre etc show calcification. 5. Goitre of the thyroid may show presence of calcifi cation in areas of degeneration. 6. Some tumours show characteristic spherules of calcification called psammoma bodies or calco spherites such as in meningioma, papillary serous cystadeno carcinoma of the ovary and papillary carci noma of the thyroid. 7. Cysts which have been present for a long time may show calcification of their walls e.g. epidermal and pilar cysts. 8. Calcinosiscutis is a condition of unknown cause in which there are irregular nodular deposits of calcium salts in the skin and subcutaneous tissue. 9. Senile degenerative changes may be accompanied by dystrophic calcification such as in costal cartilages]]>
Tue, 23 May 2023 04:19:22 GMT /slideshow/calcificationpptx/257970140 vaishaliwasnik@slideshare.net(vaishaliwasnik) Calcification.pptx vaishaliwasnik Deposition of calcium salts in tissues other than osteoid or enamel is called pathologic or heterotopic calcification Two distinct types of pathologic calcification are recognised: Dystrophic calcifi cation is characterised by deposition of calcium salts in dead or degenerated tissues with normal calcium metabolism and normal serum calcium level. Metastatic calcifi cation, on the other hand, occurs in apparently normal tissues and is associated with deranged calcium metabolism and hypercalcaemia. Etiopathogenesis The two types of pathologic calcifi cation result from distinctly different etiologies and mechanisms. DYSTROPHIC CALCIFICATION As apparent from definition, dystrophic calcification may occur due to 2 types of causes: Calcification in dead tissue. Calcification of degenerated tissue. Calcification in dead tissue Caseous necrosis in tuberculosis is the most common site for dystrophic calcification. Living bacilli may be present even in calcified tuberculous lesions, lymph nodes, lungs, etc 2. Liquefaction necrosis in chronic abscesses may get calcified. 3. Fat necrosis following acute pancreatitis or traumatic fat necrosis in the breast results in deposition of calcium soaps. 4. Gamna-Gandy bodies in chronic venous congestion (CVC) of the spleen is characterised by calcific deposits admixed with haemosiderin on fi brous tissue. 5. Infarcts may sometimes undergo dystrophic calcifi cation. 6. Th rombi, especially in the veins, may produce phleboliths. 7. Haematomas in the vicinity of bones may undergo dystrophic calcification. 8. Dead parasites like in hydatid cyst, Schistosoma eggs, and cysticercosis are some of the examples showing dystrophic calcifi cation. 9. Microcalcifi cation in breast cancer detected by mammography. 10. Congenital toxoplasmosis involving the central nervous system visualised by calcifi cation in the infant brain. Calcification in degenerated tissues 1. Dense old scars may undergo hyaline degeneration and subsequent calcifi cation. 2. Atheromas in the aorta and coronaries frequently undergo calcifi cation. 3. M旦nckebergs sclerosis shows calcifi cation in the degenerated tunica media of muscular arteries in elderly people . 4. Stroma of tumours such as uterine fi broids, breast cancer, thyroid adenoma, goitre etc show calcification. 5. Goitre of the thyroid may show presence of calcifi cation in areas of degeneration. 6. Some tumours show characteristic spherules of calcification called psammoma bodies or calco spherites such as in meningioma, papillary serous cystadeno carcinoma of the ovary and papillary carci noma of the thyroid. 7. Cysts which have been present for a long time may show calcification of their walls e.g. epidermal and pilar cysts. 8. Calcinosiscutis is a condition of unknown cause in which there are irregular nodular deposits of calcium salts in the skin and subcutaneous tissue. 9. Senile degenerative changes may be accompanied by dystrophic calcification such as in costal cartilages <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/calcification-230523041922-1e8dfa73-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Deposition of calcium salts in tissues other than osteoid or enamel is called pathologic or heterotopic calcification Two distinct types of pathologic calcification are recognised: Dystrophic calcifi cation is characterised by deposition of calcium salts in dead or degenerated tissues with normal calcium metabolism and normal serum calcium level. Metastatic calcifi cation, on the other hand, occurs in apparently normal tissues and is associated with deranged calcium metabolism and hypercalcaemia. Etiopathogenesis The two types of pathologic calcifi cation result from distinctly different etiologies and mechanisms. DYSTROPHIC CALCIFICATION As apparent from definition, dystrophic calcification may occur due to 2 types of causes: Calcification in dead tissue. Calcification of degenerated tissue. Calcification in dead tissue Caseous necrosis in tuberculosis is the most common site for dystrophic calcification. Living bacilli may be present even in calcified tuberculous lesions, lymph nodes, lungs, etc 2. Liquefaction necrosis in chronic abscesses may get calcified. 3. Fat necrosis following acute pancreatitis or traumatic fat necrosis in the breast results in deposition of calcium soaps. 4. Gamna-Gandy bodies in chronic venous congestion (CVC) of the spleen is characterised by calcific deposits admixed with haemosiderin on fi brous tissue. 5. Infarcts may sometimes undergo dystrophic calcifi cation. 6. Th rombi, especially in the veins, may produce phleboliths. 7. Haematomas in the vicinity of bones may undergo dystrophic calcification. 8. Dead parasites like in hydatid cyst, Schistosoma eggs, and cysticercosis are some of the examples showing dystrophic calcifi cation. 9. Microcalcifi cation in breast cancer detected by mammography. 10. Congenital toxoplasmosis involving the central nervous system visualised by calcifi cation in the infant brain. Calcification in degenerated tissues 1. Dense old scars may undergo hyaline degeneration and subsequent calcifi cation. 2. Atheromas in the aorta and coronaries frequently undergo calcifi cation. 3. M旦nckebergs sclerosis shows calcifi cation in the degenerated tunica media of muscular arteries in elderly people . 4. Stroma of tumours such as uterine fi broids, breast cancer, thyroid adenoma, goitre etc show calcification. 5. Goitre of the thyroid may show presence of calcifi cation in areas of degeneration. 6. Some tumours show characteristic spherules of calcification called psammoma bodies or calco spherites such as in meningioma, papillary serous cystadeno carcinoma of the ovary and papillary carci noma of the thyroid. 7. Cysts which have been present for a long time may show calcification of their walls e.g. epidermal and pilar cysts. 8. Calcinosiscutis is a condition of unknown cause in which there are irregular nodular deposits of calcium salts in the skin and subcutaneous tissue. 9. Senile degenerative changes may be accompanied by dystrophic calcification such as in costal cartilages
Calcification.pptx from vaishaliwasnik
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Morphology of cell injury and Intracellular accumulationspptx /slideshow/morphology-of-cell-injury-and-intracellular-accumulationspptx/257969778 morphologyofcellinjury-230523041019-c376b0e0
MORPHOLOGY OF REVERSIBLE CELL INJURY Common examples of morphologic forms of reversible cell injury are as under: Hydropic change 2. Hyaline change 3. Mucoid change 4. Fatty change (discussed under intracellular accumulations) 1. HYDROPIC CHANGE Hydropic change means accumulation of water within the cytoplasm of the cell. Other synonyms used are cloudy swelling (for gross appearance of the affected organ) and vacuolar degeneration (due to cytoplasmic vacuolation). Hydropic swelling is an entirely reversible change upon removal of the injurious agent. ETIOLOGY This is the commonest and earliest form of cell injury from almost all causes. The common causes include acute and subacute cell injury from various etiologic agents such as bacterial toxins, chemicals, poisons, burns, high fever, intravenous administration of hypertonic glucose or saline etc. PATHOGENESIS Cloudy swelling results from impaired regulation of sodium and potassium at the level of cell membrane. This results in intracellular accumulation of sodium and escape of potassium. This, in turn, is accompanied with rapid flow of water into the cell to maintain iso-osmotic 2. HYALINE CHANGE The word hyaline or hyalin means glassy (hyalos = glass). Hyalinisation is a common descriptive histologic term for glassy, homo geneous, eosinophilic appearance of proteinaceous material in haematoxylin and eosin-stained sections and does not refer to any specific substance. Though fibrin and amyloid have hyaline appearance, they have distinctive features and staining reactions and can be distinguished from non-specific hyaline material. Hyaline change is seen in heterogeneous pathologic conditions and may be intracellular or extracellular. INTRACELLULAR HYALINE Intracellular hyaline is mainly seen in epithelial cells. 1. Hyaline droplets in the proximal tubular epithelial cells due to excessive reabsorption of plasma proteins in proteinuria. 2. Hyaline degeneration of rectus abdominalis muscle called Zenkers degeneration, occurring in typhoid fever. The muscle loses its fi brillar staining and becomes glassy and hyaline. 3. Mallorys hyaline represents aggregates of intermediate filaments in the hepatocytes in alcoholic liver cell injury. 4. Nuclear or cytoplasmic hyaline inclusions seen in some viral infections. 5. Russells bodies representing excessive immuno glo bulins in the rough endoplasmic reticulum of the plasma cell EXTRACELLULAR HYALINE Extracellular hyaline commonly termed hyalinisation is seen in connective tissues. 1. Hyaline degeneration in leiomyomas of the uterus. 2. Hyalinised old scar of fi brocollagenous tissues. 3. Hyaline arteriolosclerosis in renal vessels in hyper tension and diabetes mellitus. 4. Hyalinised glomeruli in chronic glomerulonephritis. 5. Corpora amylacea seen as rounded masses of concentric hyaline laminae in the enlarged prostate in the elderly, in the brain and in the spinal cord in old age, and in old infarcts of the lung. ]]>

MORPHOLOGY OF REVERSIBLE CELL INJURY Common examples of morphologic forms of reversible cell injury are as under: Hydropic change 2. Hyaline change 3. Mucoid change 4. Fatty change (discussed under intracellular accumulations) 1. HYDROPIC CHANGE Hydropic change means accumulation of water within the cytoplasm of the cell. Other synonyms used are cloudy swelling (for gross appearance of the affected organ) and vacuolar degeneration (due to cytoplasmic vacuolation). Hydropic swelling is an entirely reversible change upon removal of the injurious agent. ETIOLOGY This is the commonest and earliest form of cell injury from almost all causes. The common causes include acute and subacute cell injury from various etiologic agents such as bacterial toxins, chemicals, poisons, burns, high fever, intravenous administration of hypertonic glucose or saline etc. PATHOGENESIS Cloudy swelling results from impaired regulation of sodium and potassium at the level of cell membrane. This results in intracellular accumulation of sodium and escape of potassium. This, in turn, is accompanied with rapid flow of water into the cell to maintain iso-osmotic 2. HYALINE CHANGE The word hyaline or hyalin means glassy (hyalos = glass). Hyalinisation is a common descriptive histologic term for glassy, homo geneous, eosinophilic appearance of proteinaceous material in haematoxylin and eosin-stained sections and does not refer to any specific substance. Though fibrin and amyloid have hyaline appearance, they have distinctive features and staining reactions and can be distinguished from non-specific hyaline material. Hyaline change is seen in heterogeneous pathologic conditions and may be intracellular or extracellular. INTRACELLULAR HYALINE Intracellular hyaline is mainly seen in epithelial cells. 1. Hyaline droplets in the proximal tubular epithelial cells due to excessive reabsorption of plasma proteins in proteinuria. 2. Hyaline degeneration of rectus abdominalis muscle called Zenkers degeneration, occurring in typhoid fever. The muscle loses its fi brillar staining and becomes glassy and hyaline. 3. Mallorys hyaline represents aggregates of intermediate filaments in the hepatocytes in alcoholic liver cell injury. 4. Nuclear or cytoplasmic hyaline inclusions seen in some viral infections. 5. Russells bodies representing excessive immuno glo bulins in the rough endoplasmic reticulum of the plasma cell EXTRACELLULAR HYALINE Extracellular hyaline commonly termed hyalinisation is seen in connective tissues. 1. Hyaline degeneration in leiomyomas of the uterus. 2. Hyalinised old scar of fi brocollagenous tissues. 3. Hyaline arteriolosclerosis in renal vessels in hyper tension and diabetes mellitus. 4. Hyalinised glomeruli in chronic glomerulonephritis. 5. Corpora amylacea seen as rounded masses of concentric hyaline laminae in the enlarged prostate in the elderly, in the brain and in the spinal cord in old age, and in old infarcts of the lung. ]]>
Tue, 23 May 2023 04:10:19 GMT /slideshow/morphology-of-cell-injury-and-intracellular-accumulationspptx/257969778 vaishaliwasnik@slideshare.net(vaishaliwasnik) Morphology of cell injury and Intracellular accumulationspptx vaishaliwasnik MORPHOLOGY OF REVERSIBLE CELL INJURY Common examples of morphologic forms of reversible cell injury are as under: Hydropic change 2. Hyaline change 3. Mucoid change 4. Fatty change (discussed under intracellular accumulations) 1. HYDROPIC CHANGE Hydropic change means accumulation of water within the cytoplasm of the cell. Other synonyms used are cloudy swelling (for gross appearance of the affected organ) and vacuolar degeneration (due to cytoplasmic vacuolation). Hydropic swelling is an entirely reversible change upon removal of the injurious agent. ETIOLOGY This is the commonest and earliest form of cell injury from almost all causes. The common causes include acute and subacute cell injury from various etiologic agents such as bacterial toxins, chemicals, poisons, burns, high fever, intravenous administration of hypertonic glucose or saline etc. PATHOGENESIS Cloudy swelling results from impaired regulation of sodium and potassium at the level of cell membrane. This results in intracellular accumulation of sodium and escape of potassium. This, in turn, is accompanied with rapid flow of water into the cell to maintain iso-osmotic 2. HYALINE CHANGE The word hyaline or hyalin means glassy (hyalos = glass). Hyalinisation is a common descriptive histologic term for glassy, homo geneous, eosinophilic appearance of proteinaceous material in haematoxylin and eosin-stained sections and does not refer to any specific substance. Though fibrin and amyloid have hyaline appearance, they have distinctive features and staining reactions and can be distinguished from non-specific hyaline material. Hyaline change is seen in heterogeneous pathologic conditions and may be intracellular or extracellular. INTRACELLULAR HYALINE Intracellular hyaline is mainly seen in epithelial cells. 1. Hyaline droplets in the proximal tubular epithelial cells due to excessive reabsorption of plasma proteins in proteinuria. 2. Hyaline degeneration of rectus abdominalis muscle called Zenkers degeneration, occurring in typhoid fever. The muscle loses its fi brillar staining and becomes glassy and hyaline. 3. Mallorys hyaline represents aggregates of intermediate filaments in the hepatocytes in alcoholic liver cell injury. 4. Nuclear or cytoplasmic hyaline inclusions seen in some viral infections. 5. Russells bodies representing excessive immuno glo bulins in the rough endoplasmic reticulum of the plasma cell EXTRACELLULAR HYALINE Extracellular hyaline commonly termed hyalinisation is seen in connective tissues. 1. Hyaline degeneration in leiomyomas of the uterus. 2. Hyalinised old scar of fi brocollagenous tissues. 3. Hyaline arteriolosclerosis in renal vessels in hyper tension and diabetes mellitus. 4. Hyalinised glomeruli in chronic glomerulonephritis. 5. Corpora amylacea seen as rounded masses of concentric hyaline laminae in the enlarged prostate in the elderly, in the brain and in the spinal cord in old age, and in old infarcts of the lung. <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/morphologyofcellinjury-230523041019-c376b0e0-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> MORPHOLOGY OF REVERSIBLE CELL INJURY Common examples of morphologic forms of reversible cell injury are as under: Hydropic change 2. Hyaline change 3. Mucoid change 4. Fatty change (discussed under intracellular accumulations) 1. HYDROPIC CHANGE Hydropic change means accumulation of water within the cytoplasm of the cell. Other synonyms used are cloudy swelling (for gross appearance of the affected organ) and vacuolar degeneration (due to cytoplasmic vacuolation). Hydropic swelling is an entirely reversible change upon removal of the injurious agent. ETIOLOGY This is the commonest and earliest form of cell injury from almost all causes. The common causes include acute and subacute cell injury from various etiologic agents such as bacterial toxins, chemicals, poisons, burns, high fever, intravenous administration of hypertonic glucose or saline etc. PATHOGENESIS Cloudy swelling results from impaired regulation of sodium and potassium at the level of cell membrane. This results in intracellular accumulation of sodium and escape of potassium. This, in turn, is accompanied with rapid flow of water into the cell to maintain iso-osmotic 2. HYALINE CHANGE The word hyaline or hyalin means glassy (hyalos = glass). Hyalinisation is a common descriptive histologic term for glassy, homo geneous, eosinophilic appearance of proteinaceous material in haematoxylin and eosin-stained sections and does not refer to any specific substance. Though fibrin and amyloid have hyaline appearance, they have distinctive features and staining reactions and can be distinguished from non-specific hyaline material. Hyaline change is seen in heterogeneous pathologic conditions and may be intracellular or extracellular. INTRACELLULAR HYALINE Intracellular hyaline is mainly seen in epithelial cells. 1. Hyaline droplets in the proximal tubular epithelial cells due to excessive reabsorption of plasma proteins in proteinuria. 2. Hyaline degeneration of rectus abdominalis muscle called Zenkers degeneration, occurring in typhoid fever. The muscle loses its fi brillar staining and becomes glassy and hyaline. 3. Mallorys hyaline represents aggregates of intermediate filaments in the hepatocytes in alcoholic liver cell injury. 4. Nuclear or cytoplasmic hyaline inclusions seen in some viral infections. 5. Russells bodies representing excessive immuno glo bulins in the rough endoplasmic reticulum of the plasma cell EXTRACELLULAR HYALINE Extracellular hyaline commonly termed hyalinisation is seen in connective tissues. 1. Hyaline degeneration in leiomyomas of the uterus. 2. Hyalinised old scar of fi brocollagenous tissues. 3. Hyaline arteriolosclerosis in renal vessels in hyper tension and diabetes mellitus. 4. Hyalinised glomeruli in chronic glomerulonephritis. 5. Corpora amylacea seen as rounded masses of concentric hyaline laminae in the enlarged prostate in the elderly, in the brain and in the spinal cord in old age, and in old infarcts of the lung.
Morphology of cell injury and Intracellular accumulationspptx from vaishaliwasnik
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_ADAPTIVE DISORDER.pptx /slideshow/adaptive-disorderpptx/257969641 adaptivedisorder-230523035426-945a6890
Adaptive disorders are the adjustments which the cells make in response to stresses which may be for physiologic needs (physiologic adaptation) or a response to non-lethal pathologic injury (pathologic adaptation). Such physiologic and pathologic adaptations occur by following processes. Decreasing or increasing their size i.e. atrophy and hypertrophy respectively, or by increasing their number i.e. Hyperplasia (postfi x word -trophy means nourishment; -plasia means growth of new cells). Changing the pathway of phenotypic diff eren tia tion of cells i.e. metaplasia and dysplasia (prefi x word meta- means transformation; dys- means bad development). 2. ATROPHY Reduction of the number and size of parenchymal cells of an organ or its parts which was once normal is called atrophy CAUSES Atrophy may occur from physiologic or pathologic causes: A. Physiologic atrophy ) Atrophy of lymphoid tissue with age. ii) Atrophy of thymus in adult life. iii) Atrophy of gonads after menopause. iv) Atrophy of brain with ageing. v) Osteoporosis with reduction in size of bony trabeculae due to ageing. 2. ATROPHY B. Pathologic atrophy 1. Starvation atrophy 2. Ischaemic atrophy 3. Disuse atrophy 4. Neuropathic atrophy 5. Endocrine atrophy 6. Pressure atrophy 7. Idiopathic atrophy 3.HYPERTROPHY Hypertrophy is an increase in the size of parenchymal cells resulting in enlargement of the organ or tissue, without any change in the number of cells. A. Physiologic hypertrophy Enlarged size of the uterus in Pregnancy is an example of physiologic hypertrophy as well as hyperplasia. B. Pathologic hypertrophy 1. Hypertrophy of cardiac muscle may occur in a number of cardiovasculardiseases. A few conditions producing left ventricular hypertrophy are as under: i) Systemic hypertension ii) Aortic valve disease (stenosis and insuffi ciency) iii) Mitral insuffi ciency 2.Hypertrophy of skeletal muscle e.g. hypertrophied mus cles in athletes and manual labourers. 3.Hypertrophy of smooth muscle e.g. i) Cardiac achalasia (in oesophagus) ii) Pyloric stenosis (in stomach) iii) Intestinal strictures iv) Muscular arteries in hypertension. 4. Compensatory hypertrophy may occur in an organ when the contralateral organ is removed e.g. i) Following nephrectomy on one side in a young patient, there is compensatory hypertrophy as well as hyperplasia of the nephrons of the other kidney. ii) Adrenal hyperplasia following removal of one adrenal gland 4.HYPERPLASIA Hyperplasia is an increase in the number of paren chymal cells resulting in enlargement of the organ or tissue. Physiologic hyperplasia The two most common types are hormonal and compensatory: 1. Hormonal hyperplasia i.e. hyperplasia occurring under the influence of hormonal stimulation e.g. i) Hyperplasia of female breast at puberty, during preg nancy and lactation. ii) Hyperplasia of pregnant uterus. iii) Proliferative activity of normal endometrium after a normal menstrual cycle. iv) Prostatic hyperplasia in old ]]>

Adaptive disorders are the adjustments which the cells make in response to stresses which may be for physiologic needs (physiologic adaptation) or a response to non-lethal pathologic injury (pathologic adaptation). Such physiologic and pathologic adaptations occur by following processes. Decreasing or increasing their size i.e. atrophy and hypertrophy respectively, or by increasing their number i.e. Hyperplasia (postfi x word -trophy means nourishment; -plasia means growth of new cells). Changing the pathway of phenotypic diff eren tia tion of cells i.e. metaplasia and dysplasia (prefi x word meta- means transformation; dys- means bad development). 2. ATROPHY Reduction of the number and size of parenchymal cells of an organ or its parts which was once normal is called atrophy CAUSES Atrophy may occur from physiologic or pathologic causes: A. Physiologic atrophy ) Atrophy of lymphoid tissue with age. ii) Atrophy of thymus in adult life. iii) Atrophy of gonads after menopause. iv) Atrophy of brain with ageing. v) Osteoporosis with reduction in size of bony trabeculae due to ageing. 2. ATROPHY B. Pathologic atrophy 1. Starvation atrophy 2. Ischaemic atrophy 3. Disuse atrophy 4. Neuropathic atrophy 5. Endocrine atrophy 6. Pressure atrophy 7. Idiopathic atrophy 3.HYPERTROPHY Hypertrophy is an increase in the size of parenchymal cells resulting in enlargement of the organ or tissue, without any change in the number of cells. A. Physiologic hypertrophy Enlarged size of the uterus in Pregnancy is an example of physiologic hypertrophy as well as hyperplasia. B. Pathologic hypertrophy 1. Hypertrophy of cardiac muscle may occur in a number of cardiovasculardiseases. A few conditions producing left ventricular hypertrophy are as under: i) Systemic hypertension ii) Aortic valve disease (stenosis and insuffi ciency) iii) Mitral insuffi ciency 2.Hypertrophy of skeletal muscle e.g. hypertrophied mus cles in athletes and manual labourers. 3.Hypertrophy of smooth muscle e.g. i) Cardiac achalasia (in oesophagus) ii) Pyloric stenosis (in stomach) iii) Intestinal strictures iv) Muscular arteries in hypertension. 4. Compensatory hypertrophy may occur in an organ when the contralateral organ is removed e.g. i) Following nephrectomy on one side in a young patient, there is compensatory hypertrophy as well as hyperplasia of the nephrons of the other kidney. ii) Adrenal hyperplasia following removal of one adrenal gland 4.HYPERPLASIA Hyperplasia is an increase in the number of paren chymal cells resulting in enlargement of the organ or tissue. Physiologic hyperplasia The two most common types are hormonal and compensatory: 1. Hormonal hyperplasia i.e. hyperplasia occurring under the influence of hormonal stimulation e.g. i) Hyperplasia of female breast at puberty, during preg nancy and lactation. ii) Hyperplasia of pregnant uterus. iii) Proliferative activity of normal endometrium after a normal menstrual cycle. iv) Prostatic hyperplasia in old ]]>
Tue, 23 May 2023 03:54:26 GMT /slideshow/adaptive-disorderpptx/257969641 vaishaliwasnik@slideshare.net(vaishaliwasnik) _ADAPTIVE DISORDER.pptx vaishaliwasnik Adaptive disorders are the adjustments which the cells make in response to stresses which may be for physiologic needs (physiologic adaptation) or a response to non-lethal pathologic injury (pathologic adaptation). Such physiologic and pathologic adaptations occur by following processes. Decreasing or increasing their size i.e. atrophy and hypertrophy respectively, or by increasing their number i.e. Hyperplasia (postfi x word -trophy means nourishment; -plasia means growth of new cells). Changing the pathway of phenotypic diff eren tia tion of cells i.e. metaplasia and dysplasia (prefi x word meta- means transformation; dys- means bad development). 2. ATROPHY Reduction of the number and size of parenchymal cells of an organ or its parts which was once normal is called atrophy CAUSES Atrophy may occur from physiologic or pathologic causes: A. Physiologic atrophy ) Atrophy of lymphoid tissue with age. ii) Atrophy of thymus in adult life. iii) Atrophy of gonads after menopause. iv) Atrophy of brain with ageing. v) Osteoporosis with reduction in size of bony trabeculae due to ageing. 2. ATROPHY B. Pathologic atrophy 1. Starvation atrophy 2. Ischaemic atrophy 3. Disuse atrophy 4. Neuropathic atrophy 5. Endocrine atrophy 6. Pressure atrophy 7. Idiopathic atrophy 3.HYPERTROPHY Hypertrophy is an increase in the size of parenchymal cells resulting in enlargement of the organ or tissue, without any change in the number of cells. A. Physiologic hypertrophy Enlarged size of the uterus in Pregnancy is an example of physiologic hypertrophy as well as hyperplasia. B. Pathologic hypertrophy 1. Hypertrophy of cardiac muscle may occur in a number of cardiovasculardiseases. A few conditions producing left ventricular hypertrophy are as under: i) Systemic hypertension ii) Aortic valve disease (stenosis and insuffi ciency) iii) Mitral insuffi ciency 2.Hypertrophy of skeletal muscle e.g. hypertrophied mus cles in athletes and manual labourers. 3.Hypertrophy of smooth muscle e.g. i) Cardiac achalasia (in oesophagus) ii) Pyloric stenosis (in stomach) iii) Intestinal strictures iv) Muscular arteries in hypertension. 4. Compensatory hypertrophy may occur in an organ when the contralateral organ is removed e.g. i) Following nephrectomy on one side in a young patient, there is compensatory hypertrophy as well as hyperplasia of the nephrons of the other kidney. ii) Adrenal hyperplasia following removal of one adrenal gland 4.HYPERPLASIA Hyperplasia is an increase in the number of paren chymal cells resulting in enlargement of the organ or tissue. Physiologic hyperplasia The two most common types are hormonal and compensatory: 1. Hormonal hyperplasia i.e. hyperplasia occurring under the influence of hormonal stimulation e.g. i) Hyperplasia of female breast at puberty, during preg nancy and lactation. ii) Hyperplasia of pregnant uterus. iii) Proliferative activity of normal endometrium after a normal menstrual cycle. iv) Prostatic hyperplasia in old <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/adaptivedisorder-230523035426-945a6890-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Adaptive disorders are the adjustments which the cells make in response to stresses which may be for physiologic needs (physiologic adaptation) or a response to non-lethal pathologic injury (pathologic adaptation). Such physiologic and pathologic adaptations occur by following processes. Decreasing or increasing their size i.e. atrophy and hypertrophy respectively, or by increasing their number i.e. Hyperplasia (postfi x word -trophy means nourishment; -plasia means growth of new cells). Changing the pathway of phenotypic diff eren tia tion of cells i.e. metaplasia and dysplasia (prefi x word meta- means transformation; dys- means bad development). 2. ATROPHY Reduction of the number and size of parenchymal cells of an organ or its parts which was once normal is called atrophy CAUSES Atrophy may occur from physiologic or pathologic causes: A. Physiologic atrophy ) Atrophy of lymphoid tissue with age. ii) Atrophy of thymus in adult life. iii) Atrophy of gonads after menopause. iv) Atrophy of brain with ageing. v) Osteoporosis with reduction in size of bony trabeculae due to ageing. 2. ATROPHY B. Pathologic atrophy 1. Starvation atrophy 2. Ischaemic atrophy 3. Disuse atrophy 4. Neuropathic atrophy 5. Endocrine atrophy 6. Pressure atrophy 7. Idiopathic atrophy 3.HYPERTROPHY Hypertrophy is an increase in the size of parenchymal cells resulting in enlargement of the organ or tissue, without any change in the number of cells. A. Physiologic hypertrophy Enlarged size of the uterus in Pregnancy is an example of physiologic hypertrophy as well as hyperplasia. B. Pathologic hypertrophy 1. Hypertrophy of cardiac muscle may occur in a number of cardiovasculardiseases. A few conditions producing left ventricular hypertrophy are as under: i) Systemic hypertension ii) Aortic valve disease (stenosis and insuffi ciency) iii) Mitral insuffi ciency 2.Hypertrophy of skeletal muscle e.g. hypertrophied mus cles in athletes and manual labourers. 3.Hypertrophy of smooth muscle e.g. i) Cardiac achalasia (in oesophagus) ii) Pyloric stenosis (in stomach) iii) Intestinal strictures iv) Muscular arteries in hypertension. 4. Compensatory hypertrophy may occur in an organ when the contralateral organ is removed e.g. i) Following nephrectomy on one side in a young patient, there is compensatory hypertrophy as well as hyperplasia of the nephrons of the other kidney. ii) Adrenal hyperplasia following removal of one adrenal gland 4.HYPERPLASIA Hyperplasia is an increase in the number of paren chymal cells resulting in enlargement of the organ or tissue. Physiologic hyperplasia The two most common types are hormonal and compensatory: 1. Hormonal hyperplasia i.e. hyperplasia occurring under the influence of hormonal stimulation e.g. i) Hyperplasia of female breast at puberty, during preg nancy and lactation. ii) Hyperplasia of pregnant uterus. iii) Proliferative activity of normal endometrium after a normal menstrual cycle. iv) Prostatic hyperplasia in old
_ADAPTIVE DISORDER.pptx from vaishaliwasnik
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_Respiratory Systems.pptx /slideshow/respiratory-systemspptx/257794041 respiratorysystems-230512043412-3241c683
The organs of the respiratory system are Nose Pharynx Larynx Trachea Two bronchi (one bronchus to each lung) Bronchioles and smaller air passages Two lungs and their coverings, the pleura muscles of respiration the intercostal muscles and the diaphragm. External respiration Exchange of gases between the blood and the lungs is called external respiration Internal respiration Exchange of gases between the blood and the cells internal respiration. The roof is formed by the cribriform plate of the ethmoid bone, and the sphenoid bone, frontal bone and nasal bones. The floor is formed by the roof of the mouth and con- sists of the hard palate in front and the soft palate behind. The hard palate is composed of the maxilla and palatine bones and the soft palate consists of involuntary muscle. The medial wall is formed by the septum. The lateral walls are formed by the maxilla, the ethmoid bone and the inferior conchae . The posterior wall is formed by the posterior wall of The posterior wall is formed by the posterior wall of the pharynx. The main sinuses are: maxillary sinuses in the lateral walls frontal and sphenoidal sinuses in the roof ethmoidal sinuses in the upper part of the lateral walls . Functions of Nose and nasal cavity Warming. Filtering and cleaning of air Humidification. Olfaction Functions of Pharynx Passageway for air and food. Warming and humidifying. Taste. Hearing. Protection. Speech. LARYNX The larynx is composed of several irregularly shaped cartilages attached to each other by ligaments and membranes. The main cartilages are: 1 thyroid cartilage 1 cricoid cartilage 2 arytenoid cartilages 1 epiglottis ------------------------elastic fibrocartilage. Functions of larynx Production of sound. Sound has the properties of pitch, volume and resonance. Pitch of the voice depends upon the length and tightness of the cords. At puberty, the male vocal cords begin to grow longer, hence the lower pitch of the adult male voice. Volume of the voice depends upon the force with which the cords vibrate. The greater the force of expired air the more the cords vibrate and the louder the sound emitted. Resonance, or tone, is dependent upon the shape of the mouth, the position of the tongue and the lips, the facial muscles and the air in the paranasal sinuses. Functions of larynx Speech. This occurs during expiration when the sounds produced by the vocal cords are manipulated by the tongue, cheeks and lips. Protection of the lower respiratory tract. During swallowing (deglutition) the larynx moves upwards, occluding the opening into it from the pharynx and thehinged epiglottis closes over the larynx. This ensures that food passes into the oesophagus and not into the lower respiratory passages Passageway for air. This is between the pharynx and trachea. Humidifying, filtering and warming. These continue as inspired air travels through the larynx. The trachea is composed of from 16 to 20 incomplete (C-shaped) rings o]]>

The organs of the respiratory system are Nose Pharynx Larynx Trachea Two bronchi (one bronchus to each lung) Bronchioles and smaller air passages Two lungs and their coverings, the pleura muscles of respiration the intercostal muscles and the diaphragm. External respiration Exchange of gases between the blood and the lungs is called external respiration Internal respiration Exchange of gases between the blood and the cells internal respiration. The roof is formed by the cribriform plate of the ethmoid bone, and the sphenoid bone, frontal bone and nasal bones. The floor is formed by the roof of the mouth and con- sists of the hard palate in front and the soft palate behind. The hard palate is composed of the maxilla and palatine bones and the soft palate consists of involuntary muscle. The medial wall is formed by the septum. The lateral walls are formed by the maxilla, the ethmoid bone and the inferior conchae . The posterior wall is formed by the posterior wall of The posterior wall is formed by the posterior wall of the pharynx. The main sinuses are: maxillary sinuses in the lateral walls frontal and sphenoidal sinuses in the roof ethmoidal sinuses in the upper part of the lateral walls . Functions of Nose and nasal cavity Warming. Filtering and cleaning of air Humidification. Olfaction Functions of Pharynx Passageway for air and food. Warming and humidifying. Taste. Hearing. Protection. Speech. LARYNX The larynx is composed of several irregularly shaped cartilages attached to each other by ligaments and membranes. The main cartilages are: 1 thyroid cartilage 1 cricoid cartilage 2 arytenoid cartilages 1 epiglottis ------------------------elastic fibrocartilage. Functions of larynx Production of sound. Sound has the properties of pitch, volume and resonance. Pitch of the voice depends upon the length and tightness of the cords. At puberty, the male vocal cords begin to grow longer, hence the lower pitch of the adult male voice. Volume of the voice depends upon the force with which the cords vibrate. The greater the force of expired air the more the cords vibrate and the louder the sound emitted. Resonance, or tone, is dependent upon the shape of the mouth, the position of the tongue and the lips, the facial muscles and the air in the paranasal sinuses. Functions of larynx Speech. This occurs during expiration when the sounds produced by the vocal cords are manipulated by the tongue, cheeks and lips. Protection of the lower respiratory tract. During swallowing (deglutition) the larynx moves upwards, occluding the opening into it from the pharynx and thehinged epiglottis closes over the larynx. This ensures that food passes into the oesophagus and not into the lower respiratory passages Passageway for air. This is between the pharynx and trachea. Humidifying, filtering and warming. These continue as inspired air travels through the larynx. The trachea is composed of from 16 to 20 incomplete (C-shaped) rings o]]>
Fri, 12 May 2023 04:34:12 GMT /slideshow/respiratory-systemspptx/257794041 vaishaliwasnik@slideshare.net(vaishaliwasnik) _Respiratory Systems.pptx vaishaliwasnik The organs of the respiratory system are Nose Pharynx Larynx Trachea Two bronchi (one bronchus to each lung) Bronchioles and smaller air passages Two lungs and their coverings, the pleura muscles of respiration the intercostal muscles and the diaphragm. External respiration Exchange of gases between the blood and the lungs is called external respiration Internal respiration Exchange of gases between the blood and the cells internal respiration. The roof is formed by the cribriform plate of the ethmoid bone, and the sphenoid bone, frontal bone and nasal bones. The floor is formed by the roof of the mouth and con- sists of the hard palate in front and the soft palate behind. The hard palate is composed of the maxilla and palatine bones and the soft palate consists of involuntary muscle. The medial wall is formed by the septum. The lateral walls are formed by the maxilla, the ethmoid bone and the inferior conchae . The posterior wall is formed by the posterior wall of The posterior wall is formed by the posterior wall of the pharynx. The main sinuses are: maxillary sinuses in the lateral walls frontal and sphenoidal sinuses in the roof ethmoidal sinuses in the upper part of the lateral walls . Functions of Nose and nasal cavity Warming. Filtering and cleaning of air Humidification. Olfaction Functions of Pharynx Passageway for air and food. Warming and humidifying. Taste. Hearing. Protection. Speech. LARYNX The larynx is composed of several irregularly shaped cartilages attached to each other by ligaments and membranes. The main cartilages are: 1 thyroid cartilage 1 cricoid cartilage 2 arytenoid cartilages 1 epiglottis ------------------------elastic fibrocartilage. Functions of larynx Production of sound. Sound has the properties of pitch, volume and resonance. Pitch of the voice depends upon the length and tightness of the cords. At puberty, the male vocal cords begin to grow longer, hence the lower pitch of the adult male voice. Volume of the voice depends upon the force with which the cords vibrate. The greater the force of expired air the more the cords vibrate and the louder the sound emitted. Resonance, or tone, is dependent upon the shape of the mouth, the position of the tongue and the lips, the facial muscles and the air in the paranasal sinuses. Functions of larynx Speech. This occurs during expiration when the sounds produced by the vocal cords are manipulated by the tongue, cheeks and lips. Protection of the lower respiratory tract. During swallowing (deglutition) the larynx moves upwards, occluding the opening into it from the pharynx and thehinged epiglottis closes over the larynx. This ensures that food passes into the oesophagus and not into the lower respiratory passages Passageway for air. This is between the pharynx and trachea. Humidifying, filtering and warming. These continue as inspired air travels through the larynx. The trachea is composed of from 16 to 20 incomplete (C-shaped) rings o <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/respiratorysystems-230512043412-3241c683-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> The organs of the respiratory system are Nose Pharynx Larynx Trachea Two bronchi (one bronchus to each lung) Bronchioles and smaller air passages Two lungs and their coverings, the pleura muscles of respiration the intercostal muscles and the diaphragm. External respiration Exchange of gases between the blood and the lungs is called external respiration Internal respiration Exchange of gases between the blood and the cells internal respiration. The roof is formed by the cribriform plate of the ethmoid bone, and the sphenoid bone, frontal bone and nasal bones. The floor is formed by the roof of the mouth and con- sists of the hard palate in front and the soft palate behind. The hard palate is composed of the maxilla and palatine bones and the soft palate consists of involuntary muscle. The medial wall is formed by the septum. The lateral walls are formed by the maxilla, the ethmoid bone and the inferior conchae . The posterior wall is formed by the posterior wall of The posterior wall is formed by the posterior wall of the pharynx. The main sinuses are: maxillary sinuses in the lateral walls frontal and sphenoidal sinuses in the roof ethmoidal sinuses in the upper part of the lateral walls . Functions of Nose and nasal cavity Warming. Filtering and cleaning of air Humidification. Olfaction Functions of Pharynx Passageway for air and food. Warming and humidifying. Taste. Hearing. Protection. Speech. LARYNX The larynx is composed of several irregularly shaped cartilages attached to each other by ligaments and membranes. The main cartilages are: 1 thyroid cartilage 1 cricoid cartilage 2 arytenoid cartilages 1 epiglottis ------------------------elastic fibrocartilage. Functions of larynx Production of sound. Sound has the properties of pitch, volume and resonance. Pitch of the voice depends upon the length and tightness of the cords. At puberty, the male vocal cords begin to grow longer, hence the lower pitch of the adult male voice. Volume of the voice depends upon the force with which the cords vibrate. The greater the force of expired air the more the cords vibrate and the louder the sound emitted. Resonance, or tone, is dependent upon the shape of the mouth, the position of the tongue and the lips, the facial muscles and the air in the paranasal sinuses. Functions of larynx Speech. This occurs during expiration when the sounds produced by the vocal cords are manipulated by the tongue, cheeks and lips. Protection of the lower respiratory tract. During swallowing (deglutition) the larynx moves upwards, occluding the opening into it from the pharynx and thehinged epiglottis closes over the larynx. This ensures that food passes into the oesophagus and not into the lower respiratory passages Passageway for air. This is between the pharynx and trachea. Humidifying, filtering and warming. These continue as inspired air travels through the larynx. The trachea is composed of from 16 to 20 incomplete (C-shaped) rings o
_Respiratory Systems.pptx from vaishaliwasnik
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HOMEOSTASIS.pptx /slideshow/homeostasispptx-257793706/257793706 homeostasis-230512041018-e6ecdcfd
The mechanism by which the constancy of the internal environment is maintained and ensured is called Homeostasis. The normal composition of internal environment consists of the following components WATER Water is the principal and essential constituent of the body. The total body water in a normal adult male comprises 50-70% (average 60%) of the body weight and about 10% less in a normal adult female (average 50%). Thus, the body of a normal male weighing 65 kg contains approximately 40 litres of water. The total body water (assuming average of 60%) is distributed into 2 main compartments of body fluids separated from each other by membranes freely permeable to water. i) Intracellular fluid compartment This comprises about 33% of the body weight, the bulk of which is contained in the muscles. ii) Extracellular fluid compartment This constitutes the remaining 27% of body weight containing water. Included in this are the following 4 subdivisions of extracellular fluid (ECF): a) Interstitial fluid including lymph fluid constitutes the major proportion of ECF (12% of body weight). b) Intravascular fluid or blood plasma comprises about 5% of the body weight. Plasma content is about 3 litres of fluid out of 5 litres of total blood volume. c) Mesenchymal tissues such as dense connective tissue, cartilage and bone contain body water that comprises about 9% of the body weight. d) Transcellular fluid constitutes 1% of body weight. This is the fluid contained in the secretions of secretory cells of the body e.g. skin, salivary glands, mucous membranes of alimentary and respiratory tracts, pancreas, liver and biliary tract, kidneys, gonads, thyroid, lacrimal gland and CSF. 2. ELECTROLYTES The concentration of cations (positively charged) and anions (negatively charged) is different in intracellular and extracellular fluids: . In the intracellular fluid, the main cations are potassium and magnesium and the main anions are phosphates and proteins. It has low concentration of sodium and chloride. . In the extracellular fluid, the predominant cation is sodium and the principal anions are chloride and bicarbonate. Besides these, a small proportion of non-diffusible nutrients and metabolites such as glucose and urea are present in the ECF. HYPONATRAEMIA A. Gain of Relatively More Water Than Loss of Sodium i. Excessive use of diuretics ii. Hypotonic irrigating fluid administration iii. Excessive IV infusion of 5% dextrose iv. Psychogenic polydipsia v. Large volume of beer consumption vi. Addisons disease B. Loss of Relatively More Salt Than Water i. Excessive use of diuretics ii. Renal failure (ARF, CRF) iii. Replacement of water without simultaneous salt replacement in conditions causing combined salt and water deficiency Positive feedback: Increases the original stimulus to push the variable farther e.g. in blood clotting and during the birth of a baby Homeostatic mechanisms are designed to reestablish homeostasis when there is an imbal]]>

The mechanism by which the constancy of the internal environment is maintained and ensured is called Homeostasis. The normal composition of internal environment consists of the following components WATER Water is the principal and essential constituent of the body. The total body water in a normal adult male comprises 50-70% (average 60%) of the body weight and about 10% less in a normal adult female (average 50%). Thus, the body of a normal male weighing 65 kg contains approximately 40 litres of water. The total body water (assuming average of 60%) is distributed into 2 main compartments of body fluids separated from each other by membranes freely permeable to water. i) Intracellular fluid compartment This comprises about 33% of the body weight, the bulk of which is contained in the muscles. ii) Extracellular fluid compartment This constitutes the remaining 27% of body weight containing water. Included in this are the following 4 subdivisions of extracellular fluid (ECF): a) Interstitial fluid including lymph fluid constitutes the major proportion of ECF (12% of body weight). b) Intravascular fluid or blood plasma comprises about 5% of the body weight. Plasma content is about 3 litres of fluid out of 5 litres of total blood volume. c) Mesenchymal tissues such as dense connective tissue, cartilage and bone contain body water that comprises about 9% of the body weight. d) Transcellular fluid constitutes 1% of body weight. This is the fluid contained in the secretions of secretory cells of the body e.g. skin, salivary glands, mucous membranes of alimentary and respiratory tracts, pancreas, liver and biliary tract, kidneys, gonads, thyroid, lacrimal gland and CSF. 2. ELECTROLYTES The concentration of cations (positively charged) and anions (negatively charged) is different in intracellular and extracellular fluids: . In the intracellular fluid, the main cations are potassium and magnesium and the main anions are phosphates and proteins. It has low concentration of sodium and chloride. . In the extracellular fluid, the predominant cation is sodium and the principal anions are chloride and bicarbonate. Besides these, a small proportion of non-diffusible nutrients and metabolites such as glucose and urea are present in the ECF. HYPONATRAEMIA A. Gain of Relatively More Water Than Loss of Sodium i. Excessive use of diuretics ii. Hypotonic irrigating fluid administration iii. Excessive IV infusion of 5% dextrose iv. Psychogenic polydipsia v. Large volume of beer consumption vi. Addisons disease B. Loss of Relatively More Salt Than Water i. Excessive use of diuretics ii. Renal failure (ARF, CRF) iii. Replacement of water without simultaneous salt replacement in conditions causing combined salt and water deficiency Positive feedback: Increases the original stimulus to push the variable farther e.g. in blood clotting and during the birth of a baby Homeostatic mechanisms are designed to reestablish homeostasis when there is an imbal]]>
Fri, 12 May 2023 04:10:17 GMT /slideshow/homeostasispptx-257793706/257793706 vaishaliwasnik@slideshare.net(vaishaliwasnik) HOMEOSTASIS.pptx vaishaliwasnik The mechanism by which the constancy of the internal environment is maintained and ensured is called Homeostasis. The normal composition of internal environment consists of the following components WATER Water is the principal and essential constituent of the body. The total body water in a normal adult male comprises 50-70% (average 60%) of the body weight and about 10% less in a normal adult female (average 50%). Thus, the body of a normal male weighing 65 kg contains approximately 40 litres of water. The total body water (assuming average of 60%) is distributed into 2 main compartments of body fluids separated from each other by membranes freely permeable to water. i) Intracellular fluid compartment This comprises about 33% of the body weight, the bulk of which is contained in the muscles. ii) Extracellular fluid compartment This constitutes the remaining 27% of body weight containing water. Included in this are the following 4 subdivisions of extracellular fluid (ECF): a) Interstitial fluid including lymph fluid constitutes the major proportion of ECF (12% of body weight). b) Intravascular fluid or blood plasma comprises about 5% of the body weight. Plasma content is about 3 litres of fluid out of 5 litres of total blood volume. c) Mesenchymal tissues such as dense connective tissue, cartilage and bone contain body water that comprises about 9% of the body weight. d) Transcellular fluid constitutes 1% of body weight. This is the fluid contained in the secretions of secretory cells of the body e.g. skin, salivary glands, mucous membranes of alimentary and respiratory tracts, pancreas, liver and biliary tract, kidneys, gonads, thyroid, lacrimal gland and CSF. 2. ELECTROLYTES The concentration of cations (positively charged) and anions (negatively charged) is different in intracellular and extracellular fluids: . In the intracellular fluid, the main cations are potassium and magnesium and the main anions are phosphates and proteins. It has low concentration of sodium and chloride. . In the extracellular fluid, the predominant cation is sodium and the principal anions are chloride and bicarbonate. Besides these, a small proportion of non-diffusible nutrients and metabolites such as glucose and urea are present in the ECF. HYPONATRAEMIA A. Gain of Relatively More Water Than Loss of Sodium i. Excessive use of diuretics ii. Hypotonic irrigating fluid administration iii. Excessive IV infusion of 5% dextrose iv. Psychogenic polydipsia v. Large volume of beer consumption vi. Addisons disease B. Loss of Relatively More Salt Than Water i. Excessive use of diuretics ii. Renal failure (ARF, CRF) iii. Replacement of water without simultaneous salt replacement in conditions causing combined salt and water deficiency Positive feedback: Increases the original stimulus to push the variable farther e.g. in blood clotting and during the birth of a baby Homeostatic mechanisms are designed to reestablish homeostasis when there is an imbal <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/homeostasis-230512041018-e6ecdcfd-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> The mechanism by which the constancy of the internal environment is maintained and ensured is called Homeostasis. The normal composition of internal environment consists of the following components WATER Water is the principal and essential constituent of the body. The total body water in a normal adult male comprises 50-70% (average 60%) of the body weight and about 10% less in a normal adult female (average 50%). Thus, the body of a normal male weighing 65 kg contains approximately 40 litres of water. The total body water (assuming average of 60%) is distributed into 2 main compartments of body fluids separated from each other by membranes freely permeable to water. i) Intracellular fluid compartment This comprises about 33% of the body weight, the bulk of which is contained in the muscles. ii) Extracellular fluid compartment This constitutes the remaining 27% of body weight containing water. Included in this are the following 4 subdivisions of extracellular fluid (ECF): a) Interstitial fluid including lymph fluid constitutes the major proportion of ECF (12% of body weight). b) Intravascular fluid or blood plasma comprises about 5% of the body weight. Plasma content is about 3 litres of fluid out of 5 litres of total blood volume. c) Mesenchymal tissues such as dense connective tissue, cartilage and bone contain body water that comprises about 9% of the body weight. d) Transcellular fluid constitutes 1% of body weight. This is the fluid contained in the secretions of secretory cells of the body e.g. skin, salivary glands, mucous membranes of alimentary and respiratory tracts, pancreas, liver and biliary tract, kidneys, gonads, thyroid, lacrimal gland and CSF. 2. ELECTROLYTES The concentration of cations (positively charged) and anions (negatively charged) is different in intracellular and extracellular fluids: . In the intracellular fluid, the main cations are potassium and magnesium and the main anions are phosphates and proteins. It has low concentration of sodium and chloride. . In the extracellular fluid, the predominant cation is sodium and the principal anions are chloride and bicarbonate. Besides these, a small proportion of non-diffusible nutrients and metabolites such as glucose and urea are present in the ECF. HYPONATRAEMIA A. Gain of Relatively More Water Than Loss of Sodium i. Excessive use of diuretics ii. Hypotonic irrigating fluid administration iii. Excessive IV infusion of 5% dextrose iv. Psychogenic polydipsia v. Large volume of beer consumption vi. Addisons disease B. Loss of Relatively More Salt Than Water i. Excessive use of diuretics ii. Renal failure (ARF, CRF) iii. Replacement of water without simultaneous salt replacement in conditions causing combined salt and water deficiency Positive feedback: Increases the original stimulus to push the variable farther e.g. in blood clotting and during the birth of a baby Homeostatic mechanisms are designed to reestablish homeostasis when there is an imbal
HOMEOSTASIS.pptx from vaishaliwasnik
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